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Ischaemic heart disease represents the most common of the serious health problems in the contemporary society and acute myocardial infarction (AMI) is the major cause of cardiovascular morbidity and death. The accurate localization and determination of the infarct size and the volume of myocardium at risk at the time of insult is crucial and vital for the choice of treatment. Initially the ischaemic cells are reversibly injured. However, if these changes are not reverted at the earliest, it results in the death of the myocyte. This irreversible myocyte necrosis travels transmurally towards epicardium in the form of a wavefront. A timely intervention during evolving infarct could reduce and delimit the infarct and preserve the left ventricular function. Enzyme analysis and electrocardiography (ECG) along with the clinical history of the patient is still considered to constitute a reliable triad in the diagnosis of myocardial infarction (MI). Efforts have been made to relate infarct size with the serum enzyme level changes without much success. In addition, a number of specialist techniques such as planar radioisotope imaging, single photon emission computed tomography (SPECT), positron emission tomography (PET), Echocardiography, Ventriculography and nuclear magnetic resonance (NMR) imaging have been devised to support diagnosis in the patients who show ambiguous symptoms and ECG findings. However most of these procedures are unavailable to the patients due to economic reasons while others have suffered due to non-availability of ideal radiopharmaceuticals. Major advances have been made in the methods based on immunological techniques to improve the detection and estimation of infarct. These methods are exclusively based upon the production and availability of specific antibodies against intracellular, cardiac specific components.

The present study was carried out to determine the possible use of cTn-I in the cardiac myofibrillar architecture, as a potential target for in vivo radioimmunodetection of cardiac damage in a brain death pig model. Radioiodination of the anti-cTn-I 5F4 McAb was carried out by lactoperoxidase method. The percentage iodine incorporation achieved was 70-75%. The radioiodinated McAbs were purified on Sephadex G-25 column and characterised by Paper chromatography, Phast Gel electrophoresis and electroimmunoblotting. Radioiodinated anti-cTn-I 5F4 McAbs were employed alongside Pyrophosphate (Tc99m-PPi) and Thallium201 chloride (Tl201) in 24 landrace pigs (brain-dead = 18 & sham-operated = 6). The percentage cardiac uptake of the radiolabelled antibody injected dose was significantly higher in the brain dead animals (0.196%) as compared to that of sham-operated animals (0.11%). Specific in vivo localization of radiolabelled McAbs in the infarcted cardiac tissue was confirmed by computer-aided reconstruction of 3-D images of the isolated heart. The preliminary results of the study revealed preferential uptake of radiolabelled antibody at the site of myocyte damage resulting from artificially induced brain death.

Cardiac troponin-I (cTn-I) was isolated from bovine left ventricular tissue and used as immunogen. Sixteen murine hybridoma lines were produced with two of them. I D 12 and 5F4, showing a high specificity for cTn-I; both of these monoclonal antibodies (McAbs) were isotyped as IgG I with kappa - light chains. The specificity of the McAbs for cTn-1 was confirmed by ELISA, western blotting and by the ability of the antibodies to block actomyosin ATPase inhibition by cTn-I. The McAbs may be useful for human ill vivo imaging of myocardial infarcts and other pathological conditions related to cardiac myocyte damage.

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